tbuckley/cabot-search huggingface dataset:
<i>Staphylococcus aureus</i> skin colonization promotes SLE-like autoimmune inflammation via neutrophil activation and the IL-23/IL-17 axis
Authors: Hitoshi Terui, Kenshi Yamasaki, Moyuka Wada-Irimada, Mayuko Onodera-Amagai, Naokazu Hatchome, Masato Mizuashi, Riu Yamashita, Takeshi Kawabe, Naoto Ishii, Takaaki Abe, Yoshihide Asano, Setsuya Aiba
Journal: Science Immunology (2022)

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by inflammation of various organs such as skin, kidneys, bones, and brain and the presence of autoantibodies. Although the cause of SLE is not completely understood, environmental factors, genetic susceptibility, hormone factors, and environmental factors are thought to play essential roles in the pathogenesis of SLE. Among environmental factors, the microbiota are linked to the development of different autoimmune diseases. The microbiota in the nasal cavity and gut are involved in SLE development, but the influence of skin microbiota is still unclear. Here, we demonstrated that epithelial cell–specific IκBζ-deficient ( Nfkbiz ΔK5 ) mice showed spontaneous skin inflammation with increased abundance of Staphylococcus aureus on the skin. When S. aureus was epicutaneously applied on Nfkbiz ΔK5 mice, Nfkbiz ΔK5 mice developed SLE-associated autoantibodies, anti-dsDNA antibodies, anti-Sm antibodies, and glomerulonephritis with IgG deposition. Epicutaneous S. aureus application significantly increased staphylococcal colonization on the skin of Nfkbiz ΔK5 mice with reduced expression of several antimicrobial peptides in the skin. This staphylococcal skin colonization promoted caspase-mediated keratinocyte apoptosis and neutrophil activation, inducing the interleukin-23 (IL-23)/IL-17 immune response by activating dendritic cells and T cells. Furthermore, the subcutaneous administration of anti–IL-23p19 and anti–IL-17A antibodies alleviated the systemic autoimmune response. Together, these findings underscore epithelial-immune cross-talk disturbances caused by skin dysbiosis as an essential mediator inducing autoimmune diseases.
Frequency and severity of respiratory infections prior to COPD diagnosis and risk of subsequent postdiagnosis COPD exacerbations and mortality: EXACOS-UK health care data study
Authors: Hannah Whittaker, Clementine Nordon, Annalisa Rubino, Tamsin Morris, Yang Xu, Enrico De Nigris, Hana Müllerová, Jennifer K Quint
Journal: Thorax (2022)

Objective Little is known about how lower respiratory tract infections (LRTIs) before chronic obstructive pulmonary disease (COPD) are associated with future exacerbations and mortality. We investigated this association in patients with COPD in England. Methods Clinical Practice Research Datalink Aurum, Hospital Episode Statistics and Office of National Statistics data were used. Start of follow-up was patient’s first ever COPD diagnosis date and a 1-year baseline period prior to start of follow-up was used to find mild LRTIs (general practice (GP) events/no antibiotics), moderate LRTIs (GP events+antibiotics) and severe LRTIs (hospitalised). Patients were categorised as having: none, 1 mild only, 2+ mild only, 1 moderate, 2+ moderate and 1+ severe. Negative binomial regression modelled the association between baseline LRTIs and subsequent COPD exacerbations and Cox proportional hazard regression was used to investigate mortality. Results In 215 234 patients with COPD, increasing frequency and severity of mild and moderate LRTIs were associated with increased rates of subsequent exacerbations compared with no recorded LRTIs (1 mild adjusted IRR 1.16, 95% CI 1.14 to 1.18, 2+ mild IRR 1.51, 95% CI 1.46 to 1.55, 1 moderate IRR 1.81, 95% CI 1.78 to 1.85, 2+ moderate IRR 2.55, 95% CI 2.48 to 2.63). Patients with 1+ severe LRTI (vs no baseline LRTIs) also showed an increased rate of future exacerbations (adjusted IRR 1.75, 95% CI, 1.70 to 1.80). This pattern of association was similar for risk of all-cause and COPD-related mortality; however, patients with 1+ severe LRTIs had the highest risk of all-cause and COPD mortality. Conclusion Increasing frequency and severity of LRTIs prior to COPD diagnosis were associated with increasing rates of subsequent exacerbations, and increasing risk of all-cause and COPD-related mortality.
Transcriptional atlas of the human immune response to 13 vaccines reveals a common predictor of vaccine-induced antibody responses
Authors: Thomas Hagan, Bram Gerritsen, Lewis E. Tomalin, Slim Fourati, Matthew P. Mulè, Daniel G. Chawla, Dmitri Rychkov, Evan Henrich, Helen E. R. Miller, Joann Diray-Arce, Patrick Dunn, Audrey Lee, A. Deckhut-Augustine, R. Gottardo, E. K. Haddad, D. A. Hafler, E. Harris, D. Farber, S. H. Kleinstein, O. Levy, J. McElrath, R. R. Montgomery, B. Peters, B. Pulendran, A. Rahman, E. F. Reed, N. Rouphael, M. M. Sarwal, R. P. Sékaly, A. Fernandez-Sesma, A. Sette, K. Stuart, A. Togias, J. S. Tsang, Ofer Levy, Raphael Gottardo, Minne M. Sarwal, John S. Tsang, Mayte Suárez-Fariñas, Rafick-Pierre Sékaly, Steven H. Kleinstein, Bali Pulendran
Journal: Nature Immunology (2022)
Engineered anti-PDL1 with IFNα targets both immunoinhibitory and activating signals in the liver to break HBV immune tolerance
Authors: Chao-Yang Meng, Shiyu Sun, Yong Liang, Hairong Xu, Chao Zhang, Min Zhang, Fu-Sheng Wang, Yang-Xin Fu, Hua Peng
Journal: Gut (2022)

Objective The purpose of this study is to develop an anti-PDL1-based interferon (IFN) fusion protein to overcome the chronic hepatitis B virus (HBV)-induced immune tolerance, and combine this immunotherapy with a HBV vaccine to achieve the functional cure of chronic hepatitis B (CHB) infection. Design We designed an anti-PDL1-IFNα heterodimeric fusion protein, in which one arm was derived from anti-PDL1 antibody and the other arm was IFNα, to allow targeted delivery of IFNα into the liver by anti-PDL1 antibody. The effect of the anti-PDL1-IFNα heterodimer on overcoming hepatitis B surface antigen (HBsAg) vaccine resistance was evaluated in chronic HBV carrier mice. Results The anti-PDL1-IFNα heterodimer preferentially targeted the liver and resulted in viral suppression, the PD1/PDL1 immune checkpoint blockade and dendritic cell activation/antigen presentation to activate HBsAg-specific T cells, thus breaking immune tolerance in chronic HBV carrier mice. When an HBsAg vaccine was administered soon after anti-PDL1-IFNα heterodimer treatment, we observed strong anti-HBsAg antibody and HBsAg-specific T cell responses for efficient HBsAg clearance in chronic HBV carrier mice that received the combination treatment but not in those that received either single treatment. Conclusions Targeting the liver with an engineered anti-PDL1-IFNα heterodimer can break HBV-induced immune tolerance to an HBsAg vaccine, offering a promising translatable therapeutic strategy for the functional cure of CHB.
Pan-vaccine analysis reveals innate immune endotypes predictive of antibody responses to vaccination
Authors: Slim Fourati, Lewis E. Tomalin, Matthew P. Mulè, Daniel G. Chawla, Bram Gerritsen, Dmitry Rychkov, Evan Henrich, Helen E. R. Miller, Thomas Hagan, Joann Diray-Arce, Patrick Dunn, Alison Deckhut-Augustine, Elias K. Haddad, David A. Hafler, Eva Harris, Donna Farber, Julie McElrath, Ruth R. Montgomery, Bjoern Peters, Adeeb Rahman, Elaine F. Reed, Nadine Rouphael, Ana Fernandez-Sesma, Alessandro Sette, Kenneth D. Stuart, Alkis Togias, Ofer Levy, Raphael Gottardo, Minnie M. Sarwal, John S. Tsang, Mayte Suárez-Fariñas, Bali Pulendran, Steven H. Kleinstein, Rafick-Pierre Sékaly
Journal: Nature Immunology (2022)

Several studies have shown that the pre-vaccination immune state is associated with the antibody response to vaccination. However, the generalizability and mechanisms that underlie this association remain poorly defined. Here, we sought to identify a common pre-vaccination signature and mechanisms that could predict the immune response across 13 different vaccines. Analysis of blood transcriptional profiles across studies revealed three distinct pre-vaccination endotypes, characterized by the differential expression of genes associated with a pro-inflammatory response, cell proliferation, and metabolism alterations. Importantly, individuals whose pre-vaccination endotype was enriched in pro-inflammatory response genes known to be downstream of nuclear factor-kappa B showed significantly higher serum antibody responses 1 month after vaccination. This pro-inflammatory pre-vaccination endotype showed gene expression characteristic of the innate activation state triggered by Toll-like receptor ligands or adjuvants. These results demonstrate that wide variations in the transcriptional state of the immune system in humans can be a key determinant of responsiveness to vaccination.
Extended<i>Knee Control</i>programme lowers weekly hamstring, knee and ankle injury prevalence compared with an adductor strength programme or self-selected injury prevention exercises in adolescent and adult amateur football players: a two-armed cluster-randomised trial with an additional comparison arm
Authors: Hanna Lindblom, Sofi Sonesson, Kalle Torvaldsson, Markus Waldén, Martin Hägglund
Journal: British Journal of Sports Medicine (2022)

Objective To evaluate the preventive efficacy of an extended version of the Knee Control injury prevention exercise programme (IPEP) compared with an adductor strength programme and to a comparison group using a self-selected IPEP in amateur adolescent and adult male and female football players. Methods Two-armed cluster-randomised trial with an additional non-randomised arm. All 251 amateur teams (players 14–46 years) in one regional football district were approached. Teams meeting inclusion criteria were randomised to (1) extended Knee Control or (2) an adductor strength programme. Teams already using an IPEP were allocated to a comparison group and received no new intervention. Players responded to weekly questionnaires about football exposures and injuries during a 7-month season. Results Seventeen teams in the extended Knee Control , 12 in the adductor and 17 in the comparison group participated, with 502 players. For the primary outcomes, no difference in injury incidence in three lower-limb injury locations combined (hamstring, knee and ankle) was seen between extended Knee Control and the adductor group, whereas extended Knee Control had 29% lower incidence than the comparison group (incidence rate ratio 0.71, 95% CI 0.52 to 0.98). No between-group differences in groin injury incidence were seen. The weekly injury prevalence rates in the three lower limb locations combined (hamstring, knee and ankle) were 17% lower (prevalence rate ratio (PRR) 0.83, 95% CI 0.69 to 1.00) and 26% lower (PRR 0.74, 95% CI 0.63 to 0.87) in extended Knee Control compared with the adductor and comparison groups, respectively. Conclusion No difference in injury incidence was seen between the extended Knee Control and the adductor programme whereas extended Knee Control reduced injury incidence by nearly one-third compared with a self-selected IPEP. Players in extended Knee Control had lower injury prevalence compared with an adductor or self-selected IPEP. Trial registration number NCT04272047 ; Clinical trials.
Epigenetics in glaucoma: a link between DNA methylation and neurodegeneration
Authors: Wendy W. Liu, Yang Sun
Journal: Journal of Clinical Investigation (2022)

Normal-tension glaucoma is a form of optic nerve degeneration that is characterized by loss of retinal ganglion cells independent of eye pressure elevation. In this issue of the JCI, Pan et al. report the discovery in a Japanese family of a mutation in the METTL23 gene, which encodes a histone arginine methyltransferase that causes normal-pressure glaucoma in haploinsufficiency. Inherited as an autosomal dominant condition, METTL23 deficiency revealed an important function in the regulation of pS2 and the downstream NF-κB signaling pathway, which has previously been linked to glaucomatous optic nerve degeneration. These findings are the first direct link between defective epigenetic regulatory machinery and genetic forms of optic nerve degeneration.
R-spondin 3 governs secretory differentiation in the gastric oxyntic glands
Authors: Ken Kurokawa, Timothy C. Wang, Yoku Hayakawa
Journal: Journal of Clinical Investigation (2022)

The gastric oxyntic glands are maintained by gastric stem cells that continuously supply all differentiated cell types within the corpus epithelium. Stem cells are supported by stromal cells that make up the stem cell niche. In this issue of the JCI, Fischer et al. report on their use of genetically engineered mouse models and organoids to study the role of R-spondin 3 (RSPO3) in the stomach. RSPO3, one of the major stem cell niche factors, primarily promoted secretory differentiation in the normal stomach, but also contributed to regeneration following injury. Mechanistically, RSPO3 was upregulated in the stroma by loss of chief cells and then activated the YAP pathway in gastric stem and progenitor cells, which appeared to be critical for regeneration of the secretory lineage. These data substantially advance our understanding of the regulation of gastric stem cells and highlight a function for RSPO3 in the gastrointestinal tract, which is as the gatekeeper of secretory differentiation.
Risk of advanced fibrosis in first-degree relatives of patients with nonalcoholic fatty liver disease
Authors: Nobuharu Tamaki, Noora Ahlholm, Panu K. Luukkonen, Kimmo Porthan, Suzanne R. Sharpton, Veeral Ajmera, Yuko Kono, Shravan Dave, Aijaz Ahmed, Vinay Sundaram, Michael J. Wilkinson, Heather Patton, Hersh Gupta, Vanessa Cervantes, Christie Hernandez, Scarlett J. Lopez, Ria Loomba, Amanda Baumgartner, Lisa Richards, Perttu E.T. Arkkila, Katriina Nemes, Helena Isoniemi, Hannele Yki-Järvinen, Rohit Loomba
Journal: Journal of Clinical Investigation (2022)

BACKGROUNDA pilot, single-center study showed that first-degree relatives of probands with nonalcoholic fatty liver disease (NAFLD) cirrhosis have a high risk of advanced fibrosis. We aimed to validate these findings using 2 independent cohorts from the US and Europe.METHODSThis prospective study included probands with NAFLD with advanced fibrosis, NAFLD without advanced fibrosis, and non-NAFLD, with at least 1 first-degree relative. A total of 396 first-degree relatives - 220 in a derivation cohort and 176 in a validation cohort - were enrolled in the study, and liver fibrosis was evaluated using magnetic resonance elastography and other noninvasive imaging modalities. The primary outcome was prevalence of advanced fibrosis in first-degree relatives.RESULTSPrevalence of advanced fibrosis in first-degree relatives of probands with NAFLD with advanced fibrosis, NAFLD without advanced fibrosis, and non-NAFLD was 15.6%, 5.9%, and 1.3%, respectively (P = 0.002), in the derivation cohort, and 14.0%, 2.6%, and 1.3%, respectively (P = 0.004), in the validation cohort. In multivariable-adjusted logistic regression models, age of ≥50 years (adjusted OR [aOR]: 2.63, 95% CI 1.0-6.7), male sex (aOR: 3.79, 95% CI 1.6-9.2), diabetes mellitus (aOR: 3.37, 95% CI 1.3-9), and a first-degree relative with NAFLD with advanced fibrosis (aOR: 11.8, 95% CI 2.5-57) were significant predictors of presence of advanced fibrosis (all P &lt; 0.05).CONCLUSIONFirst-degree relatives of probands with NAFLD with advanced fibrosis have significantly increased risk of advanced fibrosis. Routine screening should be done in the first-degree relatives of patients with advanced fibrosis.FUNDINGSupported by NCATS (5UL1TR001442), NIDDK (U01DK061734, U01DK130190, R01DK106419, R01DK121378, R01DK124318, P30DK120515, K23DK119460), NHLBI (P01HL147835), and NIAAA (U01AA029019); Academy of Finland grant 309263; the Novo Nordisk, EVO, and Sigrid Jusélius Foundations; and the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement 777377. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation program and the EFPIA.
A clinical-grade liquid biomarker detects neuroendocrine differentiation in prostate cancer
Authors: Shuang G. Zhao, Jamie M. Sperger, Jennifer L. Schehr, Rana R. McKay, Hamid Emamekhoo, Anupama Singh, Zachery D. Schultz, Rory M. Bade, Charlotte N. Stahlfeld, Cole S. Gilsdorf, Camila I. Hernandez, Serena K. Wolfe, Richel D. Mayberry, Hannah M. Krause, Matt Bootsma, Kyle T. Helzer, Nicholas Rydzewski, Hamza Bakhtiar, Yue Shi, Grace Blitzer, Christos E. Kyriakopoulos, David Kosoff, Xiao X. Wei, John Floberg, Nan Sethakorn, Marina Sharifi, Paul M. Harari, Wei Huang, Himisha Beltran, Toni K. Choueiri, Howard I. Scher, Dana E. Rathkopf, Susan Halabi, Andrew J. Armstrong, David J. Beebe, Menggang Yu, Kaitlin E. Sundling, Mary-Ellen Taplin, Joshua M. Lang
Journal: Journal of Clinical Investigation (2022)

BackgroundNeuroendocrine prostate cancer (NEPC) is an aggressive subtype, the presence of which changes the prognosis and management of metastatic prostate cancer.MethodsWe performed analytical validation of a Circulating Tumor Cell (CTC) multiplex RNA qPCR assay to identify the limit of quantification (LOQ) in cell lines, synthetic cDNA, and patient samples. We next profiled 116 longitudinal samples from a prospectively collected institutional cohort of 17 patients with metastatic prostate cancer (7 NEPC, 10 adenocarcinoma) as well as 265 samples from 139 patients enrolled in 3 adenocarcinoma phase II trials of androgen receptor signaling inhibitors (ARSIs). We assessed a NEPC liquid biomarker via the presence of neuroendocrine markers and the absence of androgen receptor (AR) target genes.ResultsUsing the analytical validation LOQ, liquid biomarker NEPC detection in the longitudinal cohort had a per-sample sensitivity of 51.35% and a specificity of 91.14%. However, when we incorporated the serial information from multiple liquid biopsies per patient, a unique aspect of this study, the per-patient predictions were 100% accurate, with a receiver-operating-curve (ROC) AUC of 1. In the adenocarcinoma ARSI trials, the presence of neuroendocrine markers, even while AR target gene expression was retained, was a strong negative prognostic factor.ConclusionOur analytically validated CTC biomarker can detect NEPC with high diagnostic accuracy when leveraging serial samples that are only feasible using liquid biopsies. Patients with expression of NE genes while retaining AR-target gene expression may indicate the transition to neuroendocrine differentiation, with clinical characteristics consistent with this phenotype.FundingNIH (DP2 OD030734, 1UH2CA260389, R01CA247479, and P30 CA014520), Department of Defense (PC190039 and PC200334), and Prostate Cancer Foundation (Movember Foundation - PCF Challenge Award).
Inflammation fuels bone marrow exhaustion caused by Samd9l mutation
Authors: Moonjung Jung
Journal: Journal of Clinical Investigation (2022)

Sterile α motif domain-containing 9 (SAMD9) and SAMD9-like (SAMD9L) syndromes are inherited bone marrow failure syndromes known for their frequent development of myelodysplastic syndrome with monosomy 7. In this issue of the JCI, Abdelhamed, Thomas, et al. report a mouse model with a hematopoietic cell-specific heterozygous Samd9l mutation knockin. This mouse model resembles human disease in many ways, including bone marrow failure and the nonrandom loss of the mutant allele. Samd9l-mutant hematopoietic stem progenitor cells showed reduced fitness at baseline, which was further exacerbated by inflammation. TGF-β hyperactivation was found to underlie reduced fitness, which was partially rescued by a TGF-β inhibitor. These findings illustrate the potential role of TGF-β inhibitors in the treatment of SAMD9/SAMD9L syndromes.
Novel Troponin Fragmentation Assay to Discriminate Between Troponin Elevations in Acute Myocardial Infarction and End-Stage Renal Disease
Authors: K.E. Juhani Airaksinen, Rami Aalto, Tapio Hellman, Tuija Vasankari, Akseli Lahtinen, Saara Wittfooth
Journal: Circulation (2022)
Platelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells
Authors: Tarun Tyagi, Kanika Jain, Timur O. Yarovinsky, Michael Chiorazzi, Jing Du, Cecilia Castro, Jules Griffin, Asawari Korde, Kathleen A. Martin, Shervin S. Takyar, Richard A. Flavell, Abhijit A. Patel, John Hwa
Journal: The Journal of Experimental Medicine (2022)

Current understanding of tumor immunosuppressive mechanisms forms the basis for modern day immunotherapies. Immunoregulatory role of platelets in cancer remains largely elusive. Platelets from non-small cell lung cancer (NSCLC) patients revealed a distinct activation phenotype. TREM-like transcript 1 (TLT-1), a platelet protein, was increased along with enhanced extracellular release from NSCLC platelets. The increased platelet TLT-1 was also evident in humanized mice with patient-derived tumors. In immunocompetent mice with syngeneic tumors, TLT-1 binding to T cells, in vivo, led to suppression of CD8 T cells, promoting tumor growth. We identified direct interaction between TLT-1 and CD3ε on T cells, implicating the NF-κB pathway in CD8 T cell suppression. Anti–TLT-1 antibody rescued patients’ T cells from platelet-induced suppression ex vivo and reduced tumors in mice in vivo. Clinically, higher TLT-1 correlated with reduced survival of NSCLC patients. Our findings thus identify TLT-1 as a platelet-derived immunosuppressor that suppresses CD8 T cells and demonstrate its therapeutic and prognostic significance in cancer.
Correction: Broader Epstein–Barr virus–specific T cell receptor repertoire in patients with multiple sclerosis
Authors: Tilman Schneider-Hohendorf, Lisa Ann Gerdes, Béatrice Pignolet, Rachel Gittelman, Patrick Ostkamp, Florian Rubelt, Catarina Raposo, Björn Tackenberg, Marianne Riepenhausen, Claudia Janoschka, Christian Wünsch, Florence Bucciarelli, Andrea Flierl-Hecht, Eduardo Beltrán, Tania Kümpfel, Katja Anslinger, Catharina C. Gross, Heidi Chapman, Ian Kaplan, David Brassat, Hartmut Wekerle, Martin Kerschensteiner, Luisa Klotz, Jan D. Lünemann, Reinhard Hohlfeld, Roland Liblau, Heinz Wiendl, Nicholas Schwab
Journal: The Journal of Experimental Medicine (2022)

During data analysis for a follow-up project, the authors found that the number of patients who received ocrelizumab infusions in the metadata underlying Fig. S3 E was incorrect.The corrected Fig. S3 with the revised panel E is provided here, and the legend has been changed as indicated in bold.In addition, in Table 1, the validation cohort data in the "Anti-CD20: before/after treatment" row now read "14/14" instead of "25/17" (shown in red text here).The conclusions regarding these data are unchanged.
Reply to Wu et al.
Authors: Noriko Nishiyama, Hideki Kobara
Journal: Endoscopy (2022)

See also: Efficacy of endoscopic ligation with O-ring closure for prevention of bleeding after gastric endoscopic submucosal dissection under antithrombotic therapy: a prospective observational studyEndoscopy 2022; 54(11): 1078-1084DOI: 10.1055/a-1782-3448 See also: Endoscopic ligation technique with O-ring closure: improved or complicated?Endoscopy 2022; 54(11): 1125-1125DOI: 10.1055/a-1901-8594
High efficacy of Azacitidine plus HAG in acute myeloid leukemia: an open-label, single-arm, multi-center, phase 2 study
Authors: Jun Li, Qi Han, Yanqing Huang, Yanhui Wei, Jie Zi, Lidong Zhao, Zhimei Cai, Xuzhang Lu, Rong Xiao, Yanming Zhang, Xiaotian Yang, Hao Xu, Naitong Sun, Wanchuan Zhuang, Zhengdong Wu, Yuan Xia, Yanli Xu, Bin He, Wei Zhu, Fengling Min, Yongchun Chen, Banghe Ding, Peimin Shi, Jing Xie, Hua Tang, Zefa Liu, Bingzong Li, Yu Sun, Hongxia Qiu, Limin Duan, Elanora Dovat, Chunhua Song, Laszlo SzeKely, Sinisa Dovat, Zheng Ge
Journal: Blood Cancer Journal (2022)
Comparative efficacy of omega-3 polyunsaturated fatty acids on major cardiovascular events: A network meta-analysis of randomized controlled trials
Authors: Bo Yang, Ping-Tao Tseng, Xiang Hu, Bing-Yan Zeng, Jane Pei-Chen Chang, Yang Liu, Wei-Jie Chu, Shuang-Shuang Zhang, Zhi-Liang Zhou, Chih-Sheng Chu, Cheng-Ho Chang, Yu-Kang Tu, Yi-Cheng Wu, Brendon Stubbs, Andre F. Carvalho, Pao-Yen Lin, Yutaka J. Matsuoka, Mein-Woei Suen, Kuan-Pin Su
Journal: Progress in Lipid Research (2022)